The Monitored Atherosclerosis Regression Study - MARS

Oct 04, 2004
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Date Published:
01/01/1993
Date Updated:
10/04/2004
Original Posted Date:
10/04/2004
References

Description:

Lovastatin for angiographic progression in CAD.

Hypothesis:

Whether lowering lipid levels consistently inhibits or reverses the development of coronary artery lesions, influences cardiac and all-cause morbidity and mortality, and offers a prudent use of medical resources.

Study Design

Study Design:

Patients Screened: Not given
Patients Enrolled: 270
Mean Follow Up: 2.2 years
Mean Patient Age: 58
Female: 9

Patient Populations:

< 70 years old.
Coronary artery disease in at least two segments, with at least one segment showing diameter stenosis of 50% or more (but not total occlusion).
Unaltered by percutaneous transluminal coronary angioplasty (PTCA).

Exclusions:

Hypertension (diastolic blood pressure >115 mmHg or, if the patient was receiving treatment, >100 mmHg)
Diabetes mellitus.
Use of lipid-lowering drugs within two months of randomization.
Premenopausal, unless surgically sterilized.
Candidates for coronary artery bypass surgery (CABG), but not candidates for PTCA.

Primary Endpoints:

Per-patient change in percent diameter stenosis as determined by quantitative coronary angiography.

Secondary Endpoints:

Global change score, based on the consensus of blinded expert readers regarding angiographic change.

Drug/Procedures Used:

Lovastatin, 40 mg bid; diet, daily cholesterol intake < 250mg, < 27% of calories as fat, saturated fat constituting < 7% of total fat calories, monounsaturated and polyunsaturated fats each accounting for < 10% of fat calories.

Principal Findings:

Lovastatin lowered total cholesterol level by 32%, low-density lipoprotein cholesterol by 38%, and the apolipoprotein B by 26% and raised the high-density lipoprotein cholesterol by 8.5% (P < 0.001).

Average percent diameter stenosis increased 2.2% in placebo recipients and 1.6% in lovastatin recipients (P > 0.20).

For lesions 50% or greater, average percent diameter stenosis increased 0.9% in placebo recipients and decreased 4.1% in lovastatin recipients (P = 0.005).

The mean global change score was +0.9 (indicating progression) in the placebo group and +0.4 in the lovastatin group (P = 0.002); 13 placebo recipients and 28 lovastatin recipients had global change scores indicating regression.

Interpretation:

Treatment with lovastatin plus diet slows the rate of progression and increases the frequency of regression in coronary artery lesions (by global change score), especially in more severe lesions (by quantitative angiography). This is the third lipid-lowering trial to show a benefit using the global change score, an end point predictive of clinical coronary events. Differences between two of these trials, using quantitative coronary angiographic endpoints, may have theoretical bearing on the mechanisms by which lipid-lowering therapy operates at the level of the arterial wall.

References:

1. Ann Intern Med 1993;119:969-76. Final results
2. Arteriosclerosis, Thromb & Vasc Biol 1996;16:697-704. Lipoprotein subclasses

Keywords: Lipoproteins, LDL, Cholesterol, Coronary Artery Disease, Lovastatin, Coronary Angiography, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Diet, Constriction, Pathologic, Lipoproteins, HDL, Angioplasty, Balloon, Coronary


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